Cytomegalovirus (CMV) disease is caused by human cytomegalovirus, a double-stranded DNA virus of the Herpesviridae family. While primary CMV infection is often asymptomatic in immunocompetent individuals, the virus can cause severe disease in neonates and immunocompromised patients. CMV is the most common cause of congenital viral infection in the United States, and a major pathogen in solid organ and hematopoietic stem cell transplant recipients.
CMV is transmitted via bodily fluids, sexual contact, organ transplantation, blood transfusions, and vertically from mother to fetus. After primary infection, the virus establishes lifelong latency, primarily in monocytes and progenitor cells, and may reactivate during periods of weakened cell-mediated immunity. Reactivation can occur spontaneously or following immunosuppressive therapy, particularly in transplant recipients, leading to systemic infection.
In congenital CMV disease, the virus crosses the placenta during maternal viremia, especially in primary infections during the first trimester. The resulting fetal infection may lead to jaundice, petechiae, hepatosplenomegaly, microcephaly, hearing loss, and periventricular calcifications. In adults, reactivation may cause pneumonia, retinitis, colitis, or encephalitis in immunosuppressed patients, while immunocompetent individuals may develop a mononucleosis-like illness that is heterophile-antibody negative.
CMV evades immune surveillance through multiple mechanisms. It interferes with MHC class I antigen presentation, preventing CD8⁺ T cell-mediated cytolysis, and secretes proteins that bind host chemokines, impairing immune cell recruitment. Additionally, CMV microRNAs suppress translation of MHC-related proteins, further inhibiting immune recognition.
Diagnosis of CMV disease relies on serologic assays (including IgM and IgG avidity) and molecular tests such as PCR for viral load assessment. Antiviral agents like ganciclovir, valganciclovir, foscarnet, and cidofovir are used for treatment, particularly in high-risk populations. No vaccine is currently available, although several candidates are under investigation.
Cytomegalovirus disease is caused by infection with a herpesvirus belonging to the genus Cytomegalovirus.
In humans, the virus can spread through infected body fluids, such as during blood transfusion, organ transplant, sexual contact, or from mother to fetus.
Once inside the body, the virus establishes latency primarily in monocytes and hematopoietic progenitor cells.
During active infection, it interferes with MHC class I antigen presentation, preventing CD8⁺ T cells from recognizing and eliminating infected cells.
Some viral proteins attach to host chemokines, hindering the recruitment of immune cells to the infection site.
Together, these mechanisms allow the virus to persist within host cells.
When a person's immunity is weakened, such as after an organ transplant, the virus may become active again.
It takes over the host cell to produce and release new virions, spreading the infection.
Virus-infected cells, especially in epithelial tissues, become enlarged and develop characteristic intranuclear inclusion bodies, which are visible under a microscope.
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